Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chloroquine is currently the drug of choice for treatment of acute attacks of Plasmodium falciparum malaria in chloroquine-sensitive areas. In areas of low level resistance, this drug may still be used (25 mg/kg of body weight in three days) in semi-immune patients. In case of failure, or in areas of high level resistance, quinine (25 mg/kg/day for 3 to 5 days) or, in spite of increasing resistance, Fansidar should be prescribed. Mefloquine, Fansimef and Halofantrine ought to be strictly prescribed to delay occurrence of resistance. Severe attacks require quinine by continuous intravenous infusion. Spleen enlargement does not usually require specific treatment unless poor tolerance is observed. Blood transfusions present a considerable risk of HIV transmission. Appropriate malaria treatment may avoid blood transfusions thus preventing HIV dissemination in Africa.
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PMID:[Treatment of Plasmodium falciparum malaria in Africa (except cerebral malaria)]. 219 75

Forty cases of imported malaria (1978 to 1988) are reviewed and management principles are discussed. All 15 cases of Plasmodium falciparum malaria were acquired in Africa, 5 of which were probably chloroquine-resistant. Most cases of Plasmodium vivax (80%) were acquired on the Indian subcontinent, including 2 cases of congenital malaria. Six children developed P. falciparum malaria despite chemoprophylaxis. All children had a history of fever, usually with other influenza-like symptoms. Two-thirds had splenomegaly, and one-third were afebrile on admission. Thrombocytopenia (70%) and anemia (70%) were often present. Forty-five percent received previous wrong diagnoses and treatments. Quinine or quinidine with either Fansidar or clindamycin were used to treat P. falciparum malaria. Clindamycin may be more effective if given for 7 instead of 3 days. There were no deaths or residual complications. As the prevalence and severity of drug-resistant P. falciparum spreads, prophylaxis and treatment choices become more difficult. Diagnosis requires a travel history and a high index of suspicion.
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PMID:Review of 40 children with imported malaria. 259 48

56 patients carriers of Plasmodium falciparum were observed throughout 1987: 47 males and 9 females of a mean age of 32. The following clinical aspects were observed: Falciparum malaria: 35 cases, malaria with a low parasitaemia (less than 1,000 HPM): 5 cases, tropical splenomegaly syndrome: 3 cases, isolated bi- or tricytopenia: 10 cases, cerebral malaria: 1 case, asymptomatic carriers: 2 cases. Statistically speaking, no significant correlation was observed between parasitaemia and the following clinical and biological symptoms: fever, splenomegaly, Hb level, platelet count. However, we noted a level of parasitaemia higher in the acute forms of malaria (Falciparum malaria and cerebral malaria) than in the non typical forms (chronic visceral malaria, haematological disorders). All asymptomatic carriers, who represent "malaria infection", presented a low parasitaemia (less than 1,000 HPM).
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PMID:[Current clinical aspects and role of parasitic density in the manifestations of falciparum malaria]. 266 7

We present two cases of Plasmodium falciparum malaria contracted in Douala despite adequate prophylaxis by Fansidar for one and by chloroquine for the other. Failure of curative treatment by Fansidar for the first case (in vitro chloroquine-resistant strain) and by amodiaquine plus erythromycin for the second. After these therapeutic failures, both patients presented without fever, but with splenomegaly and anaemia. The successful therapeutic was mefloquine.
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PMID:[2 cases of multiresistant Plasmodium falciparum malaria contracted in Douala with atypical clinical presentation]. 331 53

An investigation of malariometric indices in relation to immunoglobulin levels, rheumatoid factors, and antithyroglobulins was carried out on 78 members of the Arfak tribe near Manokwari in Western New Guinea, in the course of a WHO assessment of malaria control activities in that region. The population investigated had been exposed to a period of epidemic malaria, as indicated by the small differences in malariometric indices between consecutive age groups. Typically high spleen sizes were recorded, as found generally among Papuans in similar situations. Falciparum malaria was most prevalent, almost equal to cases of vivax and malariae malaria together. IgM levels were very high, while those of IgG, IgA and IgD were not elevated. Total serum protein was rather low. No correlation between malariometric indices, autoantibodies, and immunoglobulin levels could be found. In particular there was no correlation between IgM levels and spleen indices, such as has been found in many other surveys. It is suggested that splenomegaly may show no correlation with the IgM level in Papuan populations without previous selection.
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PMID:Immuno-epidemiology of malaria: a study in a tribal area of West Irian. 421 Oct 55

What were first called simply false-positive Wassermann reactions and then lupus anticoagulant are now known as antiphospholipid or anticardiolipin antibodies (ACA). These are known to cause a tendency to thrombosis and are frequently present in many neurological conditions and infections. The pathological significance of these antibodies in acute infections, if any, is unknown. We investigated the presence of these antibodies in Plasmodium falciparum malaria in an endemic area in Natal/KwaZulu, and attempted to correlate the presence of this antibody with cerebral manifestations. Immunoglobulin G-anticardiolipin antibodies measured by enzyme-linked immunosorbent assay occurred significantly more frequently in 62 patients with acute Plasmodium falciparum malaria (33.9%) than in 37 control subjects (2.7%) (P < 0.0001). There was no significant difference in the mean parasite loads in those patients who were positive for ACA (1.75%) and those who were negative (1.59%) (P = 0.83). No correlation was found between parasite load and ACA levels in the patient group, or between the number of cerebral manifestations in patients with and without the antibody. The frequency of splenomegaly was not significantly different in patients with and without ACA (P = 0.06). We conclude that there is a high prevalence of ACA in acute falciparum malaria. The pathological significance of this antibody and its relationship to complications, especially cerebral ones, warrant greater attention and may improve the understanding of cerebral malaria and its management.
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PMID:Are anticardiolipin antibodies responsible for some of the complications of severe acute Plasmodium falciparum malaria? 831 Mar 60

Plasmodium falciparum malaria is endemic in the northern KwaZulu areas of South Africa. The clinical morbidity produced by this parasite has not been studied since the institution of the present malaria control programme. Fifty-nine patients were prospectively studied at a peripheral clinic during the peak malaria season; symptoms and signs of the infection, parasite loads, haemoglobin values and leucocyte counts were recorded in all patients. Haemoglobin and leucocyte counts were also measured in 37 control subjects without malaria. The commonest symptoms were persistent headache (100%), rigors (98%) and myalgia (93%). None of the patients presented with coma, pulmonary oedema, hypoglycaemia or algid malaria. Splenomegaly was found in 49%, hepatomegaly in 20% and mental confusion in 5% of patients. Mean parasite load was 1.71% and 57% of patients had parasite loads of < 1%. Anaemia of < 10 g/dl was significantly more frequent (P < 0.0001) in the patient group than in the control group. Leucopenia (white cell count < 4.0 x 10(9)/l) was present in 12 of 50 patients in whom it was measured compared with 2 controls (P = 0.0175). The results show a wide range of morbidity, without severe complications as presenting manifestations. Symptomatic infection in the presence of low parasite loads suggests that there may be little or no immunity in this population.
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PMID:Morbidity from falciparum malaria in Natal/KwaZulu. 845 85

Chloroquine-resistant Plasmodium falciparum malaria and human virus (HIV) infection through blood transfusions used to treat malaria-associated anemia are causes of increasing morbidity and mortality among children in Africa. To evaluate the role of malaria and other risk factors for pediatric anemia, we conducted a study of children brought to the emergency ward of a large urban hospital in Kinshasa, Zaire. A total of 748 children ages six through 59 months were enrolled; 318 (43%) children were anemic (hematocrit < 33%), including 74 (10%) who were severely anemic (hematocrit < 20%). Plasmodium falciparum parasites were detected in 166 children (22%); hematocrits for these children (mean 25.8%) were significantly lower than for aparasitemic children (mean 33.7%; P < 10(-6)). Fever with splenomegaly (odds ratio [OR] = 6.5, P = 0.02), parasitemia (OR = 3.5, P < 0.001), lower socioeconomic status (OR = 2.0, P = 0.004), and malnutrition (OR = 1.8, P = 0.06) were independently associated with anemia in a multivariate model. Recent antimalarial therapy was also associated with a lower hematocrit, suggesting that chloroquine may have aggravated the anemia. A reassessment of the effectiveness of strategies to diagnose and treat malaria and malnutrition is necessary to decrease the high prevalence of anemia and the resultant high rate of blood transfusions in areas endemic for malaria and HIV.
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PMID:Plasmodium falciparum-associated anemia in children at a large urban hospital in Zaire. 847 Jul 74

A major epidemic of Plasmodium falciparum malaria occurred in a nonimmune population in northeastern Kenya during January-May 1998. The epidemic was preceded by drought in 1996 and most of 1997, then by major rainfall and floods in the last 2 months of 1997. A two-stage cluster-sampling survey conducted at mobile clinics in Wajir, Kenya, in 1988, retrospectively assessed malaria prevalence and mortality. From February 14 to May 3, 1998, a total of 23,377 malaria cases (attack rate, 38.9%) were reported. Average daily crude mortality was 9.4/10,000 and daily under-5 mortality was 28.4/10,000. The most common drugs administered to patients presenting to mobile units were chloroquine and pyrimethamine. The positive predictive values of clinical signs of malaria in relation to parasitemia stage were higher among patients with temperatures above 37.5 degrees Celsius (65%) or splenomegaly (46%). 380 cases of severe malaria were admitted to the malaria treatment unit for a mean stay of 2.3 days; 31 of these patients died (case fatality ratio, 8.2%). The epidemic's severity was aggravated by late recognition and a lack of preparedness.
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PMID:Epidemic of malaria in north-eastern Kenya. 980 79

Between January and December 1996, we observed 64 children (mean age 8.3 years range 4.2 to 11.2 years) who required dialysis for severe acute renal failure secondary to Falciparum Malaria. All received anti malarial therapy and other supportive therapy as well as peritoneal dialysis. Out of these 28 died (43.8%). The children who died (Group I) compared to those who survived (Group II) differed significantly in age (mean +/- SD) (7.2 +/- 1.3 years vs. 9.2 +/- 2.1 years P < 0.05), plasma creatinine at presentation (645 +/- 104 mumol/L vs. 438 +/- 87 mumol/L P < 0.05), plasma bilirubin (2.1 +/- 0.3 mg/dL vs. 1.2 +/- 0.2 mg/dL P > 0.02) systolic BP (50 +/- 11 mmHg vs. 90 +/- 12 mmHg P0 < 0.01), diastolic BP (20 +/- 4 mmHg vs. 60 +/- 9 mmHg P < .01) .Hb level 5.3 +/- 0.4 g/dL vs. 8 +/- 1.3 gm/dL P < .02), time from diagnosis to referral (5.3 +/- 1.3 days vs. 8.9 +/- 2.1 days P < .05) and urine output (200 +/- 49 mL/24 h vs. 600 mL +/- 131 mL P < .01). There was no significant difference in gender, alanine transaminase (ALT) level, degree of fever, plasma Na or plasma K. Diarrhea was present in 29% of the children who died and in only 11% of those who survived (P > 0.05) and splenomegaly was found in 3% and 18% respectively (PO > .05).
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PMID:Prognosis of malaria associated severe acute renal failure in children. 1004 18


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